Through the use of an in vitro model system this study proposes to elucidate the mechanism(s) by which bacterial endotoxin(s), an etiologic agent in periodontal disease, directly (in the absence of the controlling and modifying influences of the host) influences connective tissue metabolism, at the cellular level, in both the diabetic and non-diabetic. Recent data have shown that ascorbic acid is protective against endotoxin, in vitro. The competitive uptake characteristics of ascorbic acid and glucose will be investigated - expecially in the diabetic - to determine whether the basic defect in the endotoxin - diabetic cell response is related to a transport phenomenon. The effect of these variables on macromolecular synthesis will be determined to see whether the rampant nature of periodontal disease in diabetes is related to a deficiency in ascorbic acid uptake in endotoxin - challanged tissues in diabetics.